Suppression of Aurora-A-FLJ10540 signaling axis prohibits the malignant state of head and neck cancer

Chen, Chang Han; Chang, Alice Y.W.; Li, Shau Hsuan; Tsai, Hann-Huei; Shiu, Li Yen; Su, Li; Wang, Wen Lung; Chiu, Tai Jen; Luo, Sheng‐Dean; Huang, Tai Lin; Chien, Chih‐Yen

doi:10.1186/s12943-015-0348-7

Cited by 15 publications

(15 citation statements)

References 37 publications

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“…To determine the value of the JMJD3 intervention in the treatment of glioma, we first examined the expression of JMJD3. Taken similar strategies with Chen et al [ 12 ], we performed data mining and analyzed JMJD3 expressions from the publicly available Oncomine database. In the database, JMJD3 was obviously up-regulated in tumor tissues of glioblastoma compared with normal brain tissues ( P <0.05, Figure 1 ).…”

Section: Resultsmentioning

confidence: 99%

The pharmacological role of histone demethylase JMJD3 inhibitor GSK-J4 on glioma cells

Sui

et al. 2017

Oncotarget

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Glioma is regarded as the most prevalent malignant carcinoma of the central nervous system, and lack of effective treatment. Thus, the development of new therapeutic strategies targeting glioma is of significant clinical importance. In the present study, histone H3K27 demethylase jumonji domain-containing protein 3 (JMJD3) was investigated as target for glioma treatment. The mRNA of JMJD3 was overexpressed in glioblastoma tissues compared to normal brain tissues (P<0.05). The content of JMJD3 was also higher in glioma cells than in human brain microvascular endothelial cell (hCMEC), and the corresponding level of H3K27me3 was decreased (P<0.05). The treatment with JMJD3 specific inhibitor GSK-J4 can increase the content of H3K27me3 in glioma cells, which means the activity of JMJD3 was inhibited. GSK-J4 can inhibit glioma cell proliferation in a concentration dependent and time-dependent manner (P<0.05). GSK-J4 also induced glioma cell apoptosis and inhibited cell migration (P<0.05). But there was no obvious effect of GSK-J4 on hCMEC cells. All together, these data suggest that GSK-J4 has important potential in the gliomas treatment.

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Section: Resultsmentioning

confidence: 99%

The pharmacological role of histone demethylase JMJD3 inhibitor GSK-J4 on glioma cells

Sui

et al. 2017

Oncotarget

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“…Colony formation assay was performed according to Park et al ’s work [ 19 , 20 ]. Both HSC-T6 and LX-2 cells were seeded (2 × 10 3 cells/well) in a 6-well plate and incubated at 37 °C under a 5 % CO 2 atmosphere for 14 days.…”

Section: Methodsmentioning

confidence: 99%

Saikosaponin d induces cell death through caspase-3-dependent, caspase-3-independent and mitochondrial pathways in mammalian hepatic stellate cells

Chen

Huang

et al. 2016

BMC Cancer

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BackgroundSaikosaponin d (SSd) is one of the main active triterpene saponins in Bupleurum falcatum. It has a steroid-like structure, and is reported to have pharmacological activities, including liver protection in rat, cell cycle arrest and apoptosis induction in several cancer cell lines. However, the biological functions and molecular mechanisms of mammalian cells under SSd treatment are still unclear.MethodsThe cytotoxicity and apoptosis of hepatic stellate cells (HSCs) upon SSd treatment were discovered by MTT assay, colony formation assay and flow cytometry. The collage I/III, caspase activity and apoptotic related genes were examined by quantitative PCR, Western blotting, immunofluorescence and ELISA. The mitochondrial functions were monitored by flow cytometry, MitoTracker staining, ATP production and XF24 bioenergetic assay.ResultsThis study found that SSd triggers cell death via an apoptosis path. An example of this path might be typical apoptotic morphology, increased sub-G1 phase cell population, inhibition of cell proliferation and activation of caspase-3 and caspase-9. However, the apoptotic effects induced by SSd are partially blocked by the caspase-3 inhibitor, Z-DEVD-FMK, suggesting that SSd may trigger both HSC-T6 and LX-2 cell apoptosis through caspase-3-dependent and independent pathways. We also found that SSd can trigger BAX and BAK translocation from the cytosol to the mitochondria, resulting in mitochondrial function inhibition, membrane potential disruption. Finally, SSd also increases the release of apoptotic factors.ConclusionsThe overall analytical data indicate that SSd-elicited cell death may occur through caspase-3-dependent, caspase-3-independent and mitochondrial pathways in mammalian HSCs, and thus can delay the formation of liver fibrosis by reducing the level of HSCs.

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“…Aberrant amplification and/ or overexpression of Aurora-A has been reported in human malignancies. A recent study also found that suppression of Aurora-A-FLJ10540 signaling axis prohibits the malignant state of head and neck cancer [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

A potential panel of two-long non-coding RNA signature to predict recurrence of patients with laryngeal cancer

Bai

Shi²,

Wang

et al. 2017

Oncotarget

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Accumulating evidence has shown that aberrant lncRNA expression plays an oncogenic or tumor-suppressive role in the tumorigenesis of laryngeal cancer. However, the prognostic roles of lncRNAs in laryngeal cancer recurrence are still poorly understood. In this study, we obtained lncRNA expression profiles of 109 patients with laryngeal cancer by mining previously published gene expression microarray data from the Gene Expression Omnibus (GEO) and identified two lncRNAs associated with laryngeal cancer recurrence in the training dataset by using Cox regression analysis. Then these two lncRNAs were combined to a two-lncRNA signature for identifying patients at high-risk of disease recurrence. By applying this two-lncRNA signature to the testing dataset, a clear separation was observed in the survival curves between patients with low- or high-risk scores, indicating good reproducibility of this two-lncRNA signature in predicting disease-free survival of laryngeal cancer. Further analysis revealed that the prognostic value of the two-lncRNA signature was independent of other clinical features, including age, stage and grade. Subsequent gene set enrichment analysis suggested that the two-lncRNA signature was more likely to involve with GPCRs downstream signaling pathway, potassium channel pathway and aurora-A pathway. Our study demonstrated that the two-lncRNA signature may be a novel potential biomarker for prognosis of laryngeal cancer and may provide novel insights into the molecular mechanism of laryngeal cancer.

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Suppression of Aurora-A-FLJ10540 signaling axis prohibits the malignant state of head and neck cancer

Cited by 15 publications

References 37 publications

The pharmacological role of histone demethylase JMJD3 inhibitor GSK-J4 on glioma cells

The pharmacological role of histone demethylase JMJD3 inhibitor GSK-J4 on glioma cells

Saikosaponin d induces cell death through caspase-3-dependent, caspase-3-independent and mitochondrial pathways in mammalian hepatic stellate cells

A potential panel of two-long non-coding RNA signature to predict recurrence of patients with laryngeal cancer

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